We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Chronic Exposure to Polystyrene Nanoplastics Promotes Lung Cancer Progression via Activating Gluconeogenesis and Inhibiting Glycolysis
AI summary Read the abstract
Researchers found that long-term exposure to polystyrene nanoplastics promoted lung cancer cell growth and migration by reprogramming cellular metabolism. The study suggests nanoplastics activate a specific metabolic pathway through the stress-response protein ATF3, shifting energy production in ways that enhance cancer cell proliferation.
Nanoplastics (NPs) are emerging as environmental pollutants, yet their long-term impact on lung cancer progression remains largely unexplored. This study explored the influence of extended exposure to polystyrene nanoplastics (PS-NPs) on the growth and movement of A549 lung cancer cells, with particular emphasis on the molecular mechanisms involved in metabolic reprogramming. We demonstrated that prolonged exposure to PS-NPs markedly increased the ability of lung cancer cells to proliferate and migrate. Using an integrated approach combining transcriptomic profiling and C13-labeled glucose flux analysis, we observed that chronic PS-NPs exposure induced metabolic reprogramming characterized by the activation of gluconeogenesis and suppression of glycolysis. Mechanistically, PS-NPs upregulated the gluconeogenic enzyme mitochondrial phosphoenolpyruvate carboxykinase (PCK2) and downregulated enolase-1 (ENO1), a glycolytic enzyme. Notably, knockdown of PCK2 attenuated PS-NPs-induced cell proliferation and migration, underscoring its functional role. We further identified that stress-responsive activating transcription factor-3 (ATF3) serves as a crucial mediator of PCK2 and ENO1 expression. Chromatin immunoprecipitation followed by PCR (ChIP-PCR) confirmed enhanced binding of ATF3 to the promoter regions of PCK2 and ENO1 upon PS-NPs exposure. Silencing ATF3 abolished PS-NPs-induced changes in PCK2 and ENO1 expression and blocked the associated increase in cell proliferation and migration. Clinically, elevated ATF3 and PCK2 expression levels are associated with poor prognosis in patients with lung cancer. In conclusion, chronic exposure to PS-NPs promotes lung cancer progression by inducing metabolic reprogramming via ATF3-mediated regulation of PCK2 and ENO1. These findings shed light on the cancer-promoting capabilities of PS-NPs and identify the ATF3-PCK2 axis as a promising target for lung cancer therapy.
More Papers Like This
Chronic nanoplastics exposure drives lung cancer progression through ATF3/PCK2 axis-mediated rewiring of truncated gluconeogenesis
AI summary Read the abstract
Researchers found that prolonged exposure of lung cancer cells to environmentally relevant nanoplastic doses accelerates tumor progression by activating an ER stress pathway that upregulates the ATF3-PCK2 metabolic axis, rewiring cancer cell metabolism toward anabolic gluconeogenesis — identifying nanoplastics as potential environmental tumor promoters.
Polystyrene nanoplastics and lung cancer: Insights from network toxicology and mechanistic in vitro studies
AI summary Read the abstract
Network toxicology analysis identified 189 potential molecular targets linking polystyrene nanoplastic exposure to lung cancer pathways, and in vitro experiments confirmed that nanoplastics promote lung cancer cell proliferation and resistance to apoptosis via PI3K/AKT signaling.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
AI summary Read the abstract
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
Chronic polystyrene microplastics exposure promotes lung adenocarcinoma metastasis through EREG-regulated phosphorylation-dependent NF-κB activation
AI summary Read the abstract
Researchers found that chronic exposure to polystyrene microplastics significantly enhanced the migration, invasion, and proliferation of lung adenocarcinoma cells in laboratory and animal models. The microplastics activated a protein called EREG that triggered NF-kB signaling, a pathway associated with tumor progression and metastasis. The study also found that high EREG expression correlated with worse clinical outcomes in lung cancer patients, suggesting a molecular mechanism by which microplastic exposure could promote cancer spread.
Long-term exposure to nanoplastics alters molecular and functional traits related to the carcinogenic process
AI summary Read the abstract
Researchers exposed cells to polystyrene nanoplastics for six months and found that long-term exposure activated multiple molecular markers associated with cancer development, including enhanced cell migration, invasion potential, and ability to grow independently. The study suggests that chronic nanoplastic exposure may pose a carcinogenic risk, though further research is needed to confirm these findings in living organisms.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.